Lecture Topic: “Critical disabilities in surgical patients” Clinical assessment of the general condition of patients. Critical disability in surgical patients Disability syndromes

Acute respiratory failure– a syndrome based on dysfunction of external respiration, leading to insufficient oxygen supply or retention of CO2 in the body. this condition is characterized by arterial hypoxemia or hypercapnia, or both.

The etiopathogenetic mechanisms of acute respiratory disorders, as well as the manifestation of the syndrome, have many features. Unlike chronic, acute respiratory failure is a decompensated condition in which hypoxemia, hypercapnia rapidly progress, and blood pH decreases. Disturbances in the transport of oxygen and CO2 are accompanied by changes in the functions of cells and organs. Acute respiratory failure is one of the manifestations of a critical condition, in which, even with timely and correct treatment, death is possible.

Clinical forms of acute respiratory failure

Etiology and pathogenesis

Acute respiratory failure occurs when there are disturbances in the chain of regulatory mechanisms, including central regulation of respiration and neuromuscular transmission, leading to changes in alveolar ventilation - one of the main mechanisms of gas exchange. Other factors of pulmonary dysfunction include lesions of the lungs (pulmonary parenchyma, capillaries and alveoli), accompanied by significant gas exchange disorders. It should be added that the “mechanics of breathing”, that is, the work of the lungs as an air pump, can also be impaired, for example, as a result of injury or deformation of the chest, pneumonia and hydrothorax, high position of the diaphragm, weakness of the respiratory muscles and (or) airway obstruction. The lungs are a “target” organ that responds to any changes in metabolism. Mediators of critical conditions pass through the pulmonary filter, causing damage to the ultrastructure of the lung tissue. Pulmonary dysfunction of varying degrees always occurs with severe impacts - trauma, shock or sepsis. Thus, the etiological factors of acute respiratory failure are extremely extensive and varied.

In intensive care practice, there are two types of acute respiratory failure: ventilation (hypercapnic) And parenchymal (hypoxemic).

Ventilatory respiratory failure manifested by a decrease in alveolar ventilation. This form of respiratory failure is accompanied by an increase in CO2 in the blood, respiratory acidosis, and arterial hypoxemia.

Causes of ventilation respiratory failure:

 Suppression of the respiratory center by narcotic, sedative drugs, barbiturates, or in connection with diseases and (or) traumatic brain injury (heart attack, cerebral edema, increased intracranial pressure, after-effects of cerebral anoxia, coma of various etiologies);

 Impaired conduction of nerve impulses to the respiratory muscles (due to traumatic injury to the spinal cord, infection such as polio, peripheral neuritis, or neuromuscular blockade caused by muscle relaxants, myasthenia gravis and other factors);

 Weakness or dysfunction of the respiratory muscles, “fatigue” of the diaphragm is a common cause of acute respiratory failure in patients in intensive care units.

 Impaired breathing can be observed with trauma or deformation of the chest, pneumothorax, pleural effusion, or lack of excursion of the diaphragm.

Ventilation respiratory failure often occurs in the immediate postoperative period. Factors contributing to ventilation failure include obesity, old age, smoking, cachexia, and kyphoscoliosis. The increased formation of CO2 in tissues, observed during hyperthermia, hypermetabolism, mainly with carbohydrate energy supply, is not always compensated by an increased volume of pulmonary ventilation.

Parenchymal respiratory failure is characterized by the development of arterial hypoxemia against the background of reduced, normal or increased CO2 levels in the blood. It develops as a result of damage to the lung tissue, pulmonary edema, severe pneumonia, acid aspiration syndrome and many other reasons and leads to severe hypoxemia. The main pathogenetic links of this form of acute respiratory failure are pulmonary shunt (discharge of blood from right to left), discrepancy between ventilation and blood flow, and disruption of diffusion processes.

Causes of parenchymal respiratory insufficiency:

 Trauma, sepsis, systemic inflammatory reaction (released inflammatory mediators: tumor necrosis factor, proinflammatory cytokines, thromboxane, NO, arachidonic acid metabolites, impaired oxygen transport when pulmonary functional units are damaged by oxygen radicals passing through the pulmonary filter;

 Multiple organ failure syndrome (in these cases, lung damage usually occurs);

 Adult respiratory distress syndrome;

 Severe forms of pneumonia;

 Pulmonary contusion;

 Atelectasis;

 Pulmonary edema (caused by an increase in hydrostatic pressure in the pulmonary capillaries or the permeability of the capillary wall);

 Severe form of bronchial asthma;

 Pulmonary embolism;

 Massive bronchopulmonary aspiration.

The identification of two forms of acute respiratory failure is to a certain extent arbitrary. Often one form turns into another. A combination of both forms is also possible.

Clinical picture Acute respiratory failure may be erased during an external examination of the patient and even absent, but it can also be extremely pronounced.

Ventilatory respiratory failure against the background of coma caused by the action of opiates, sedative drugs, anesthesia, is accompanied by minor signs (miosis, shallow breathing). An increase in Pco2 leads to stimulation of the respiratory center, which will most likely result in an increase in all parameters of external respiration. However, this does not happen when exposed to drugs. If active oxygenation is carried out under these conditions, a further decrease in ventilation volume, even apnea, may occur. With the development of ventilation respiratory failure in a patient with initially clear consciousness, blood pressure rises (often up to 200 mmHg and above), and brain symptoms appear. Very characteristic symptoms of hypercapnia are significant sweating, bronchial hypersecretion and lethargy. If you help the patient cough and eliminate bronchial obstruction, then lethargy disappears. Hypercapnia is also characterized by oliguria, which is always observed with severe respiratory acidosis.

Decompensation of the condition occurs at the moment when the high level of Pco2 in the blood ceases to stimulate the respiratory center. Signs of decompensation in advanced cases include a sharp decrease in minute ventilation, circulatory disorders and the development of coma, which, with progressive hypercapnia, is CO2 narcosis. Pco2 in this case reaches 100 mmHg, but coma can occur earlier - due to hypoxemia. At this stage, it is necessary to carry out artificial ventilation of the lungs with high FiO2. The development of shock against the background of a coma means the beginning of rapid damage to the cellular structures of the brain, internal organs and tissues.

Parenchymal respiratory failure is often not accompanied by symptoms of respiratory failure, with the exception of changes in arterial blood tests indicating a decrease in Po2. it is characterized by a gradual or rapidly progressive course, mild clinical symptoms and the possibility of death within a short time. Initially, tachycardia develops with moderate arterial hypertension, nonspecific neurological manifestations are possible: inadequacy of thinking, confusion of consciousness and speech, lethargy, and so on. Cyanosis is a relatively subjective factor, observed only in the late stage of acute respiratory failure. And corresponding to a significant decrease in saturation and oxygen tension in arterial blood (SaO2< 80%, Po2 < 50ммHg). Внезапно нарушается сознание и развивается кома (гипоксическая) с отсутствием рефлексов, падением артериального давления, остановкой сердечной деятельности. Продолжительность гипоксемической формы острой дахательной недостаточности может колебаться от нескольких минут (при аспирации, асфиксии, синдроме Мендельсона) до нескольких часов и дней (респираторный дистресс синдром взрослых).

Clinical signs of progressive respiratory failure:

 Breathing disorders (shortness of breath, gradual decrease in tidal and minute breathing volumes, oligopnea, mild cyanosis);

 Increasing neurological symptoms (indifference, aggressiveness, agitation, lethargy, coma);

 Disorders of the cardiovascular system (tachycardia, persistent increase in blood pressure during hypercapnia, decompensation of the cardiovascular system and cardiac arrest).

Clinical signs of acute respiratory failure:

 Acute respiratory failure (oligoproe, tachypnea, bradypnea, apnea, pathological rhythms);

 Progressive respiratory hypoxemia (Po2< 50 мм Hg при дыхании воздухом);

 Progressive hypercapnia (Pco2< 50 мм Hg);

 pH< 7,30.

All these signs are not always detected. The presence of at least two of them allows a diagnosis to be made.

Acute heart failure- This is a sudden onset of muscular failure of the ventricles of the heart. This condition can be aggravated by the dissonance between the decreased functioning of one and the normal function of another part of the heart. Sudden onset of cardiac weakness can be fatal.

The causes of acute cardiac dysfunction are myocardial infarction, diffuse myocarditis, excessive physical activity, intercurrent infection, as well as other pathological conditions in which hypercatecholaminemia, a violation of the ionic composition of the intracellular fluid, conduction disturbances, especially in the atrieventricular system (Morgagni-Edams-Stokes attacks) are observed. ), disturbance of excitability (attacks of paroxysmal tachycardia, paroxysmal flutter and atrial fibrillation and ventricular fibrillation leading to asystole).

Symptoms of acute heart failure

The clinical picture of acute heart failure, accompanied by a drop in cardiac output and a sharp decrease in blood supply to the arterial system, is very reminiscent of the picture of acute vascular circulatory failure, which is why it is sometimes referred to as acute cardiac collapse, or cardiogenic shock. Patients experience extreme weakness, a state close to fainting), pallor, cyanosis, coldness of the extremities, and very low pulse filling. Recognition of acute weakness of the heart is based primarily on the detection of changes in the heart (expansion of the boundaries of the heart, arrhythmia, pre-diastolic gallop rhythm). In this case, shortness of breath, swelling of the neck veins, congestive wheezing in the lungs, and cyanosis are observed. A sharp slowdown (less than 40 per minute) or increased heart rate (more than 160 per minute) is more characteristic of cardiac weakness than vascular weakness. Blood pressure is reduced. There are symptoms of organ ischemia with symptoms of venous congestion due to the disproportion between the total mass of circulating blood and its effective volume.

Acute syndrome right ventricular failure most clearly manifested in cases of blockage of the pulmonary artery trunk or its large branch due to the introduction of a blood clot from the veins of the legs, pelvis, or less often from the right ventricle or atrium. The patient suddenly develops shortness of breath, cyanosis, sweat, a feeling of constriction or pain in the heart area, the pulse becomes very small and frequent, and blood pressure drops. Soon, if the patient remains alive, venous pressure increases, the neck veins swell, and then the liver enlarges, an accent of the second tone on the pulmonary artery and a gallop rhythm are heard. X-ray reveals an enlargement of the right ventricle and expansion of the conus of the pulmonary artery. After 1-2 days, signs of heart attack and pneumonia may appear.

Acute right ventricular failure can be observed in patients with acute myocardial infarction of the posterior wall with concomitant pneumosclerosis and pulmonary emphysema. Along with the clinical picture of myocardial infarction, they experience cyanosis, congestion in the systemic circulation, and sudden enlargement of the liver. Sometimes patients are admitted to the surgical department with a diagnosis of acute abdomen and acute cholecystitis due to severe pain in the right hypochondrium due to stretching of the liver capsule.

Acute left ventricular failure clinically manifested by cardiac asthma and pulmonary edema.

Cardiac asthma is an attack of asthma.

It should be borne in mind that the clinical picture of acute left ventricular failure also develops in cases of mechanical closure of the left atrioventricular orifice by a moving thrombus in mitral stenosis. Characteristic is the disappearance of the arterial pulse along with a noticeable strong heartbeat, the appearance of acute pain in the heart area, shortness of breath, increasing cyanosis with subsequent loss of consciousness and the development in most cases of reflex collapse. Prolonged closure of the atrioventricular orifice by a thrombus usually leads to the death of patients.

Similarly, with mitral stenosis, acute functional failure syndrome of the left atrium is often observed. This happens when the defect is compensated by increased work of the left atrium while the contractile function of the right ventricle is preserved. With excessive physical stress, sudden stagnation of blood in the vessels of the lungs can occur and an attack of cardiac asthma may occur, which can develop into acute pulmonary edema. Sometimes such attacks are repeated frequently, appear suddenly and disappear just as suddenly, which confirms the great importance of the reflex influence from the atria to the pulmonary vessels.

Until now, all the mechanisms of development of cardiac asthma have not been deciphered. Convincing data have been obtained on the role of the central and autonomic nervous systems in the occurrence of these attacks. Hormonal factors also have a big influence.

It is known that attacks of cardiac asthma and pulmonary edema can occur when the cardiac probe irritates the pulmonary artery receptors during cardiac probing.

With physical exertion, excitement, fever, pregnancy, etc., there is an increased need for oxygen in the body, increased cardiac activity and increased cardiac output, which in patients with existing heart lesions can lead to suddenly developing weakness of the left side of the heart. A decompensated difference in the ejection of blood from the right and left parts of the heart leads to overflow of the pulmonary circulation. Pathological reflexes due to hemodynamic disturbances lead to the fact that the production of glucocorticoids decreases, and mineralocorticoids increases. This, in turn, increases vascular permeability and causes sodium and water retention in the body, which further worsens hemodynamic parameters.

It is necessary to take into account one more factor that can play a big role in the development of these complications - a violation of lymph circulation in the lung tissue, expansion of the anastomoses between the veins of the large and small circle.

Long-term increase in capillary pressure in the lungs above 30 mmHg. Art. causes fluid to leak from the capillaries into the alveoli and can lead to pulmonary edema. At the same time, as shown in the experiment, a short-term increase in capillary pressure in the lungs, reaching 50 mm Hg. Art. and more, does not always lead to pulmonary edema. This indicates that capillary pressure is not the only factor influencing the development of pulmonary edema. A significant role in the development of pulmonary edema belongs to the permeability of the alveolar and capillary walls and the degree of precapillary pressure. Thickening and fibrosis of the alveolar wall may prevent the development of pulmonary edema at high capillary pressure. With increased capillary permeability (anoxemia, infections, anaphylactic shock, etc.), pulmonary edema can develop even when the capillary pressure is significantly below 30 mm Hg. Art. Pulmonary edema occurs in patients with a small difference between the pressure in the pulmonary artery and pulmonary capillaries and low pulmonary arteriolar resistance. When the pressure gradient between the pulmonary artery and the pulmonary capillaries is high, there is a high pulmonary arteriolar resistance, which creates a protective barrier that protects the pulmonary capillaries from overflowing with blood, a sharp increase in pressure in them, and, consequently, from the occurrence of cardiac asthma or pulmonary edema . In patients with pronounced narrowing of the left venous ostium, development of muscle fibers in the pulmonary arterioles, proliferation of fibrous tissue in the intima of vessels, thickening of the pulmonary capillaries, hypertrophy of the fibrous base with partial loss of elasticity of the pulmonary tissue were noted. In this regard, the pulmonary capillaries move away from the alveolar membrane, and the alveolar membranes themselves thicken. This restructuring begins when the pressure in the pulmonary artery increases to 50 mm Hg. Art. and higher and is most pronounced in the pulmonary vessels with an increase in pulmonary arterial pressure to 90 mm Hg. Art. and higher.

These changes reduce the permeability of blood vessels and alveolar membranes. However, these morphological changes in patients with mitral stenosis do not exclude the possibility of them developing attacks of suffocation or pulmonary edema. Capillary extravasation is also possible with these changes, but at a higher “critical” level of pulmonary capillary pressure necessary for the occurrence of capillary extravasation and the passage of tissue fluid through the altered alveolar membranes.

Clinic for cardiac asthma and pulmonary edema characterized initially by the occurrence of severe suffocation and severe cyanosis. A large number of scattered dry and moist rales are detected in the lungs. There is bubbling breathing, a cough with the release of foamy sputum (often blood-stained). Blood pressure often decreases.

Acute renal failure (ARF)- this is a sudden, potentially reversible, significant decrease or complete cessation of all (secretory, excretory and filtration) functions of the kidneys. Every second patient with acute renal failure needs hemodialysis. Currently, there is a trend in which acute renal failure is identified as one of the manifestations of multiple organ failure syndrome.

CAUSES

All the reasons that cause the development of acute renal failure can be divided into three large groups:

1. Extrarenal (extrarenal) causes- lead to a decrease in blood volume and a sharp decrease in renal blood flow, which can cause irreversible death of renal tissue cells. Extrarenal causes of acute renal failure include: severe extensive operations, especially in weakened or elderly patients; injuries accompanied by painful shock and hypovolemia; sepsis; massive blood transfusion; extensive burns; uncontrollable vomiting; uncontrolled use of diuretics; cardiac tamponade.

2. Renal (renal) causes– include ischemic and toxic damage to the renal tissue, acute inflammation of the renal parenchyma or damage to the renal vessels, which cause necrosis of the renal tissue. Renal causes of acute renal failure include: acute glomerulonephritis; acute tubular necrosis; rheumatic kidney damage; blood diseases; poisoning with mercury, copper, cadmium salts, poisonous mushrooms, organic fertilizers; malignant arterial hypertension; lupus nephritis; uncontrolled use of drugs from the group of sulfonamides, antitumor drugs, aminoglycosides, NSAIDs.

3. Subrenal (postrenal) causes– are associated with a violation of the outflow of urine, which leads to the accumulation of urine in the collecting system, edema and necrosis of renal tissue cells. Renal causes of acute renal failure include: bilateral obstruction of the ureters by stones or blood clots; urethritis and periurethritis; tumors of the ureters, prostate, bladder; long-term compression of the ureters during trauma, surgical interventions on the abdominal organs.

CLASSIFICATION

Depending on the causes of development, prerenal, renal and postrenal acute renal failure are distinguished, respectively.

SYMPTOMS

With acute renal failure, there is a sharp disruption of all functions performed by the kidneys. The loss of the kidneys' ability to maintain the balance of electrolytes in the blood is accompanied by an increase in the concentration of calcium and potassium ions and chlorine, as well as the accumulation of protein metabolic products and an increase in the level of urea and creatinine in the blood. Violation of the secretory function of the kidneys causes the development of anemia and thrombocytopenia. As a consequence of impaired renal excretory function, one of the main symptoms of acute renal failure develops - oliguria (decreased urine output) up to anuria (complete absence of urine). The condition of patients with acute renal failure is usually moderate or severe, disturbances of consciousness occur (lethargy or excessive agitation), swelling of the extremities, cardiac arrhythmias, nausea and vomiting, and an increase in the size of the liver is determined.

The clinical course of acute renal failure is divided into several stages, successively replacing each other.

1. At the initial stage of acute renal failure, which usually lasts several hours, less often several days, circulatory collapse develops, accompanied by severe ischemia of the renal tissue. The patient's condition may be different; it is determined by the main cause of the development of acute renal failure.

2. At the stage of oligoanuria, there is a sharp reduction in urine volume (no more than 0.5 liters of urine per day) or a complete absence of urination. This stage usually develops within three days from the onset of acute renal failure, but can extend to 5-10 days. Moreover, the later acute renal failure develops and the longer its duration, the worse the prognosis of the disease and the higher the likelihood of death. With prolonged oligoanuria, the patient becomes lethargic and lethargic, and may fall into a coma. Due to pronounced suppression of immunity, the risk of secondary infection with the development of pneumonia, stomatitis, mumps, etc. increases.

3. During the diuretic stage, there is a gradual increase in urine volume, reaching about 5 liters of urine per day. The duration of the diuretic stage is usually 10-14 days, during which a gradual regression of the symptoms of renal failure occurs and the electrolyte balance of the blood is restored.

4. At the recovery stage, further restoration of all kidney functions occurs. It may take 6 months to a year to fully restore kidney function.

Acute liver failure develops as a result of massive necrosis of hepatocytes, which leads to a sharp deterioration in liver function in patients without pre-existing liver disease. The main symptom of acute renal failure is hepatic encephalopathy (HE), which decisively influences the course of acute renal failure and the prognosis of the disease.

We can talk about acute renal failure if encephalopathy develops within 8 weeks from the onset of the first symptoms of acute hepatic cellular failure. If PE develops within 8 to 24 weeks from the onset of the first symptoms of liver damage, then we should talk about subacute liver failure. In addition, it is advisable to distinguish between hyperacute liver failure, which develops within 7 days of the onset of jaundice. Mortality in acute renal failure, according to various authors, ranges from 50 to 90%.

The main etiological factors for the development of acute renal failure are:

1. Viral hepatitis.

2. Drug poisoning (paracetamol).

3. Poisoning with hepatotoxic poisons (mushrooms, alcohol substitutes, etc.).

4. Wilson–Konovalov disease.

5. Acute fatty degeneration of the liver in pregnant women.

Main symptoms and complications of acute renal failure

Hepatic Encephalopathy is a complex of potentially reversible neuropsychiatric disorders that arise as a consequence of acute or chronic liver failure and/or portosystemic blood shunting.

According to most researchers, HE develops due to the penetration of endogenous neurotoxins through the blood-brain barrier (BBB) ​​and their effect on astroglia as a result of liver cell failure. In addition, the amino acid imbalance that occurs in liver failure affects the development of PE. As a result, the permeability of the BBB and the activity of ion channels change, neurotransmission and the supply of neurons with high-energy compounds are disrupted. These changes underlie the clinical manifestations of PE.

Hyperammonemia in liver diseases is associated with a decrease in the synthesis of urea and glutamine in the liver, as well as with portosystemic blood shunting. Ammonia in non-ionized form (1-3% of total blood ammonia) easily penetrates the BBB, stimulating the transport of aromatic amino acids into the brain, resulting in increased synthesis of false neurotransmitters and serotonin.

According to some authors, in addition to ammonia, neurotoxins involved in the pathogenesis of PE include mercaptans, short- and medium-chain fatty acids, and phenols formed from the corresponding substrates under the influence of intestinal bacteria. The mechanisms of their action are similar and are associated with inhibition of neuronal Na+,K+-ATPase and increased transport of aromatic amino acids into the brain. Short- and medium-chain fatty acids, in addition, inhibit the synthesis of urea in the liver, which contributes to hyperammonemia.

Finally, there are indications of the role of the inhibitory neurotransmitter g-aminobutyric acid (GABA) of intestinal origin in the pathogenesis of PE, the excessive supply of which to the brain under conditions of astroglial edema also leads to an increase in neuropsychic disorders characteristic of PE.

It is important to note that a clear relationship between the concentrations of each of the listed metabolites involved in the pathogenesis of PE and the severity of encephalopathy has not been established. Thus, PE appears to be the result of a complex effect and mutual reinforcement of several factors: endogenous neurotoxins, among which ammonia is of leading importance, amino acid imbalance and changes in the functional activity of neurotransmitters and their receptors.

The development of encephalopathy in patients with acute renal failure is dominated by factors of parenchymal liver failure, the outcome of which is often endogenous hepatic coma. Provoking factors in this case are the increased breakdown of proteins contained in the diet, or when blood protein enters during gastrointestinal bleeding, irrational use of medications, alcoholic excesses, surgical interventions, concomitant infections, etc. Encephalopathy in patients with cirrhosis of the liver can be episodic with spontaneous resolution or intermittent, lasting many months or even years. In accordance with the criteria of the International Association for the Study of Liver Diseases (Brighton, UK, 1992) and the standardization of nomenclature, diagnostic signs and prognosis of liver and biliary tract diseases (C. Leevy et al., 1994), latent and clinically pronounced (4 stages) PE are distinguished .

1. General symptoms of acute renal failure: nausea, vomiting, anorexia, hyperthermia, malaise and progressive fatigue.

2. Jaundice is a mirror of the degree of liver failure. Bilirubin levels may increase to 900 µmol/L.

3. “Liver odor” from the mouth (smell of rotten meat).

4. Flopping tremor. Determined in conscious patients. In addition, it can be recorded with uremia, respiratory failure, low levels of potassium in the blood plasma, as well as intoxication with a number of drugs.

5. Ascites and edema (associated with a decrease in albumin levels in the blood).

6. Deficiency of coagulation factors due to a decrease in their production by the liver. The platelet count also decreases. As a result, gastrointestinal bleeding and diapedetic bleeding from the nasopharynx, retroperitoneal space, and injection sites often develop.

7. Metabolic disorders. Typically, hypoglycemia develops as a result of gluconeogenesis and an increase in insulin levels.

8. Cardiovascular complications:

hyperdynamic circulation (reminiscent of septic shock) - increased cardiac index, low peripheral resistance, arterial hypotension;

hypovolemia;

enlarged heart;

pulmonary edema;

arrhythmias (atrial fibrillation and ventricular extrasystoles);

pericarditis, myocarditis and bradycardia develop in the terminal phase of acute liver failure.

9. Sepsis. The septic condition is enhanced by the phenomena of immunological dysfunction. The most common pathogens are Staphylococcus aureus/Streptococci, intestinal flora.

10. Renal failure (hepatorenal syndrome). Most patients with acute renal failure have renal failure, which is manifested by oliguria and increased blood creatinine levels. In cases of acetaminaphen poisoning, renal failure also develops as a result of the direct toxic effect of the drug. Tubular damage can develop as a result of hypotension and hypovolemia. Blood urea levels in acute renal failure are usually low as a result of decreased synthesis in the liver.

Differential diagnosis of acute (fulminant) liver failure should be made with bacterial meningitis, brain abscess, and encephalitis.

DISEASE - a disorder of the body's vital functions, expressed by physiological and structural changes; occurs under the influence of extraordinary (for a given organism) irritants of the external and internal environment. Environmental factors always play a leading role in the occurrence of a disease, since they not only act directly on the body, but can also cause changes in its internal properties; these changes, being passed on to offspring, may themselves later become the cause of the disease (congenital characteristics). In the body during illness, destructive processes are combined - the result of damage to certain physiological systems (nervous, circulatory, respiration, digestion, etc.) by a pathogenic factor, and restorative processes - the result of the body's counteraction to this damage (for example, increased blood flow, inflammatory reaction, fever and other). Disease processes are characterized by certain signs (symptoms) that distinguish different diseases from each other.

The body's reactions that occur in response to the influence of a pathogenic factor develop differently depending on the properties of the diseased organism. This explains the diversity of the clinical picture and course of the same disease in different individuals. At the same time, each disease has some typical symptoms and course. The branch of pathology (the study of diseases) that studies the mechanisms of disease development is called pathogenesis.

The study of the causes of disease constitutes a branch of pathology called etiology. The causes of the disease may be

1. external factors: mechanical - bruises, wounds, tissue crushing and others; physical - the effect of electric current, radiant energy, heat or cold, changes in atmospheric pressure; chemical - the effect of toxic substances (arsenic, lead, chemical warfare agents and others); biological - living pathogens (pathogenic bacteria, viruses, protozoa, single-celled organisms, worms, ticks, helminths); nutritional disorders - starvation, lack of vitamins in the diet, etc.; mental impact (for example, fear, joy, which can cause dysfunction of the nervous system, cardiovascular, gastrointestinal tract and others; careless words of a doctor can cause serious disorders in suspicious people);
2. internal properties of the body - hereditary, congenital (that is, arising as a result of intrauterine development) and acquired during the subsequent life of a person.

Social factors are extremely important in the occurrence and spread of human disease: difficult working and living conditions of the working masses in a number of capitalist and colonial countries, chronic unemployment, overwork and exhaustion are factors that reduce the body’s resistance and contribute to the spread of the disease and the occurrence of early disability; lack of labor protection leads to the development of severe diseases; wars, which cause injuries and deaths of millions of people, are also the cause of an increase in morbidity among the population. In socialist countries, conditions have been created that promote maximum preservation of workers' health; special health measures at work have led to the elimination of a number of occupational diseases. The socialist health care system favors the prevention of the occurrence and rapid cure of diseases. These circumstances had a dramatic impact on the reduction of morbidity in the USSR and the increase in life expectancy of workers.

During each disease, three periods are distinguished: latent, or hidden; period of precursors, or prodromal; period of severe illness.

• The first, latent period - the time from the onset of action of the pathogenic agent to the appearance of the first symptoms of the disease in infectious diseases; this period is called the incubation period); Its duration varies for different diseases - from several minutes (for example, a burn) to several years (for example, ).
• The second, prodromal period is the time when the first, often unclear, general symptoms of the disease are detected - general malaise, headache, slight rise in temperature.
• The third period, which comes after the prodromal period, is the main one in the course of the disease and is characterized by pronounced symptoms typical of the disease; Its duration varies for different diseases - from several days to tens of years (for example, tuberculosis, syphilis, leprosy). A number of diseases have a definite course (for example, typhoid fever, relapsing fever, pneumonia and others), other diseases do not have such a definite course. Based on the course of the disease and its most characteristic manifestations, the doctor usually makes a diagnosis.

Often, during the course of the disease, complications arise - the appearance of new additional dysfunctions of individual organs or systems (for example, pneumonia in measles, inflammation of the testicle in mumps, bedsores in long-term chronic diseases, in these cases you need to know how to use an anti-bedsore mattress. Sometimes during the course of the disease they arise relapses - the return of the disease after a period of apparent recovery (for example, with typhoid fever, erysipelas, and others).

The outcome of the disease can be: recovery, that is, complete restoration of impaired functions; incomplete recovery, disability - residual effects in the form of persistent weakening of the functions of one or another system - nervous, cardiovascular and others (for example, heart disease after articular rheumatism, immobility of a joint after a tuberculous process in it); transition to a chronic, protracted condition; death. The transition to recovery can occur quickly: a sharp drop in temperature, subsidence of symptoms of the disease - the so-called crisis. Sometimes the transition from illness to recovery occurs slowly, the symptoms of the disease disappear gradually, the temperature does not drop to normal immediately - this is the so-called lysis. Death is usually preceded by agony, lasting from several hours to several days.

Diseases are classified either depending on the damage to certain body systems (disease of the nervous system, respiratory disease, cardiovascular disease, and others) or according to causative factors (infectious diseases, traumatic diseases, nutritional disorders, and so on). In addition, diseases are classified according to the nature of their course: acute, chronic, subacute. Based on the nature of the symptoms and the course of the disease, mild and severe forms of the disease are distinguished.

Treatment of a disease consists of influencing therapeutic factors either on the causes of the disease or on the mechanisms of their development, as well as by mobilizing a number of protective and compensatory adaptations of the body.

A correct understanding of disease, primarily as a result of the interaction of the body with the external environment, determines the preventive direction of socialist health care, which aims primarily to eliminate conditions that can cause disease.

Types of depression of consciousness Fainting - generalized muscle weakness, inability to stand upright, loss of consciousness. Coma is a complete shutdown of consciousness with a total loss of perception of the environment and oneself. Collapse is a drop in vascular tone with a relative decrease in circulating blood volume.

Degrees of impairment of consciousness Stupor – unconsciousness, preservation of defensive movements in response to painful and sound stimuli. Moderate coma – inability to wake up, lack of defensive movements. Deep coma - suppression of tendon reflexes, loss of muscle tone. Terminal coma is an agonal state.

Assessment of the depth of impairment of consciousness (Glasgow scale) Clear consciousness 15 Stunning Stupor 9-12 Coma 4-8 Brain death 3

Emergency care for loss of consciousness Eliminate etiological factors. Place the patient in a horizontal position with the leg end raised. Ensure free breathing: unfasten the collar and belt. Give stimulants (ammonia, vinegar) to inhale. Rub the body, cover with warm heating pads. Inject 1% mezaton 1 ml IM or s/c 10% caffeine 1 ml. For severe hypotension and bradycardia, 0.1% atropine 0.5-1 ml.

Physiology of respiration The breathing process The breathing process is conventionally divided into 3 stages: The first stage includes the delivery of oxygen from the external environment to the alveoli. The second stage involves the diffusion of oxygen through the alveolar membrane of the acinus and its delivery to the tissues. The third stage includes the utilization of oxygen during the biological oxidation of substrates and the formation of energy in cells. If pathological changes occur at any of these stages, ARF may occur. With ARF of any etiology, there is a disruption in the transport of oxygen to tissues and the removal of carbon dioxide from the body.

Indicators of blood gases in a healthy person Indicator Arterial blood Mixed blood p O 2 mm Hg. st SaO 2, % pCO 2, mm Hg. st

Etiological classification of ARF PRIMARY (stage 1 pathology - oxygen delivery to the alveoli) Causes: mechanical asphyxia, spasm, tumor, vomit, pneumonia, pneumothorax. SECONDARY (stage 2 pathology - oxygen transport from the alveoli to the tissues is impaired) Causes: microcirculation disorders, hypovolemia, pulmonary embolism, cardiogenic pulmonary edema.

The main syndromes of ARF 1. Hypoxia is a condition that develops with a decrease in tissue oxygenation. Exogenous hypoxia - due to a decrease in the partial pressure of oxygen in the inhaled air (submarine accidents, high altitudes). Hypoxia due to pathological processes that disrupt the supply of oxygen to tissues at its partial pressure.

Hypoxia due to pathological processes is divided into: a) respiratory (alveolar hypoventilation - obstruction of the airways, reduction of the respiratory surface of the lungs, respiratory depression of central origin); b) circulatory (against the background of acute and chronic circulatory failure); c) tissue (potassium cyanide poisoning - the process of oxygen absorption by tissues is disrupted); d) hemic (decrease in red blood cell mass or hemoglobin in red blood cells).

3. Hypoxemic syndrome is a violation of oxygenation of arterial blood in the lungs. An integral indicator is a reduced level of partial oxygen tension in arterial blood, which occurs in a number of parenchymal lung diseases. Main syndromes of ARF

Clinical stages of ARF Stage I: Consciousness: preserved, anxiety, euphoria. Respiratory function: lack of air, respiratory rate per minute, mild acrocyanosis. Blood circulation: heart rate per minute. BP is normal or slightly elevated. The skin is pale and moist. Partial pressure of O 2 and CO 2 of blood: p O 2 up to 70 mm Hg. p CO 2 up to 35 mmHg.

Stage II: Consciousness: impaired, agitation, delirium. Respiratory function: severe suffocation, respiratory rate per minute. Cyanosis, sweating of the skin. Blood circulation: heart rate per minute. Blood pressure Partial pressure of O 2 and CO 2 of blood: p O 2 to 60 mm Hg. p CO 2 up to 50 mmHg. Clinical stages of ARF

Stage III: Consciousness: absent, clonic-tonic convulsions, pupils dilated, do not respond to light. Respiratory function: tachypnea 40 or more per minute turns into bradypnea 8-10 per minute, spotty cyanosis. Blood circulation: heart rate more than 140 per minute. Blood pressure, atrial fibrillation. Partial pressure of O 2 and CO 2: p O 2 up to 50 mmHg. p CO 2 to mmHg. Clinical stages of ARF

Emergency care for acute respiratory failure 1. Restoration of airway patency. 2. Elimination of alveolar ventilation disorders (local and general). 3. Elimination of central hemodynamic disorders. 4. Correction of the etiological factor of ARF. 5. Oxygen therapy 3-5 l/min. at stage I ARF. 6. At stages II – III of ARF, tracheal intubation and artificial ventilation are performed.

Treatment of AHF 1. Subcutaneous administration of 1-2 ml of morphine, preferably combined with the administration of 0.5 ml of a 0.1% solution of atropine sulfate; 2. Nitroglycerin under the tongue - 1 tablet or 1-2 drops of 1% solution on a piece of sugar; 3. Analgesics: baralgin 5.0 IV, IM, no-shpa 2.0 IM, analgin 2.0 IM. 4. For cardiac arrhythmias: lidocaine mg IV, procainamide 10% 10.0 IV, obzidan 5 mg IV. 5. For pulmonary edema: dopmin 40 mg IV on glucose, Lasix 40 mg IV, aminophylline 2.4% 10.0 IV.

ETIOLOGY OF AKI 1. Traumatic, hemorrhagic, blood transfusion, bacterial, anaphylactic, cardiogenic, burn, surgical shock; electrical trauma, postpartum sepsis, etc. 2. Acute infarction of the kidney. 3. Vascular abstraction. 4. Urological abstraction.

DIAGNOSTICS 1. Decreased diuresis (less than 25 ml/h) with the appearance of protein, red blood cells, leukocytes, casts, decreased urine density to 1.005-1, increased azotemia (16.7-20.0 mmol/l). 3. Hyperkalemia. 4. Decrease in blood pressure. 5. Decrease in hemoglobin and red blood cells.

Prevention and treatment of acute renal failure 1. Sufficient pain relief for injuries. 2. Elimination of hypovolemia. 3. Elimination of water and electrolyte disturbances. 4. Correction of cardiodynamics and rheology. 5. Correction of respiratory function. 6. Correction of metabolic disorders. 7. Improving blood supply to the kidneys and eliminating foci of infection in them. 8. Antibacterial therapy. 9. Improving rheology and microcirculation in the kidneys. 10. Extracorporeal detoxification (hemodialysis). 11. Osmodiuretics (Manitol 20% 200.0 IV), saluretics (Lasix mg IV).

Classification of acute liver disease 1. Endogenous – it is based on massive necrosis of the liver, resulting from direct damage to its parenchyma; 2. Exogenous (portocaval) – the form develops in patients with liver cirrhosis. In this case, the metabolism of ammonia by the liver is disrupted; 3. Mixed form.

CLINICAL MANIFESTATIONS OF OPEN 1. Depression of consciousness up to coma 2. Specific “liver odor” from the mouth 3. Icterus of the sclera and skin 4. Signs of hemorrhagic syndrome 5. Appearance of areas of erythema in the form of stellate angiomas 6. Jaundice 7. Ascites 8. Splenomegaly

LABORATORY DIAGNOSTICS Study of liver functions (increased bilirubin, transaminases, decreased protein), kidneys (azotemia), acid-base balance (metabolic acidosis), water and electrolyte metabolism (hypokalemia, hyponatremia), blood coagulation system (hypocoagulation).

Principles of treatment for APE 1. Eliminate bleeding and hypovolemia. 2. Eliminate hypoxia. 3. Detoxification. 4. Normalization of energy metabolism. 5. Use of hepatotropic vitamins (B 1 and B 6), hepatoprotectors (essentiale). 6. Normalization of protein metabolism. 7. Normalization of water-electrolyte metabolism, acid-base balance. 8. Normalization of the blood coagulation system.

General dysfunctions in acute surgical diseases of the abdominal organs are mainly caused by intoxication.

Endogenous intoxication- (Latin in in, inside + Greek toxikon poison) - a disruption of life caused by toxic substances formed in the body itself.

Endotoxicosis(endotoxicoses; Greek endō inside + toxikon poison + -ōsis) - complications of various diseases associated with disruption of homeostasis due to the accumulation in the body of endogenous toxic substances with pronounced biological activity. In clinical practice, endotoxemia is usually considered as a syndrome of endogenous intoxication that occurs with acute or chronic failure of the body's natural detoxification system (inability to effectively remove metabolic products). In contrast to intoxication, endotoxemia refers to an already formed state of poisoning with substances of an endogenous nature, and the term “intoxication” refers to the entire pathological process of intense self-poisoning of the body.

To refer to the processes of eliminating endotoxemia, the terms “detoxification” and “detoxification” are used. The latter term is more often used to describe therapeutic methods of enhancing the natural processes of cleansing the body.

Clinical signs of endotoxicosis have been known for a long time. In almost any disease, especially of an infectious nature, children and adults develop symptoms characteristic of “endogenous intoxication”: weakness, stupor, nausea and vomiting, loss of appetite and weight loss, sweating, pale skin, tachycardia, hypotension, etc. These most typical signs are usually divided into groups. The phenomena of neuropathy (encephalopathy), which are based on dysfunctions of the nervous system (neurotoxicosis), are often the first prodromal symptoms of developing intoxication, since the most highly differentiated nerve cells of the brain are especially sensitive to metabolic disorders and hypoxia. In children, dysfunctions of the nervous system are most severe with the development of psychomotor agitation, convulsions, soporous or even comatose states. In infectious diseases, a feverish state with signs of intoxication psychosis is typical. Manifestations of cardiovasopathy can be in the nature of mild asthenovegetative disorders and severe circulatory disorders of a hypodynamic type (decrease in stroke volume of the heart, increase in total peripheral vascular resistance, cardiac rhythm and conduction disturbances), usually accompanied by respiratory failure (shortness of breath, cyanosis of the mucous membranes, metabolic acidosis). Hepato- and nephropathy are most often manifested by proteinuria, oliguria, azotemia, and sometimes liver enlargement and jaundice are noted.

Laboratory diagnostics. To assess the severity of toxemia and monitor the dynamics of its development, quite a few laboratory tests have been proposed. One of the first to use integral indicators of blood plasma (lymph) toxicity was the leukocyte intoxication index and the neutrophil shift index.

For laboratory assessment of the severity of homeostasis disorders accompanying endotoxemia, traditional methods are used that characterize the main functions of the affected organ (for example, in case of nephropathy, the composition of urine, the concentration of creatinine, urea in plasma, etc. are examined; in case of hepatopathy, a blood test is performed for bilirubin, transaminases, proteins, cholesterol etc.) or a certain body system that usually suffers from endotoxicosis. This is primarily the acid-base state, osmolarity, rheological data (relative viscosity, aggregation of erythrocytes and platelets) and basic immunological indicators (level of T- and B-lymphocytes, immunoglobulins of class G, A, M, etc.).

Some laboratory biochemical tests are specific for this type of lesions that cause endotoxemia, for example, determination of myoglobin in the blood and urine in case of injury, enzyme activity in case of pancreatitis, bacteremia in case of sepsis.

1) etiological, which aims to accelerate the removal of toxic substances from the body using methods of enhancing natural detoxification and methods of “artificial detoxification”;

2) pathogenetic, associated with the need to reduce the intensity of catabolic processes and the activity of proteolytic enzymes, increase the immunological defense of the body;

3) symptomatic, with the task of maintaining the function of the cardiovascular and respiratory systems.

In addition, the entire arsenal of treatments for the underlying disease, which led to the development of endotoxemia, is simultaneously used. Most often this is antibacterial treatment, specific pharmacotherapy, surgical treatment, etc.

For the purpose of detoxification, intravenous infusion therapy (solutions of glucose, electrolytes, hemodez) is most widely used, often in combination with the method of forced diuresis using osmotic diuretics (urea, mannitol in a dose of 1-1.5 g/kg) in the form of hypertonic solutions (15-20%) or saluretics (furosemide in a dose of up to 500-800 mg per day).

To remove toxins from the blood, hemofiltration is used ( hemodialysis )or hemosorption, as well as plasmapheresis surgery (purification of blood plasma). In cases of overhydration of the body or high concentrations of toxins in the blood and lymph, it is recommended lymphatic drainage and cleansing the resulting lymph (lymphosorption) with its subsequent return to the body (intravenous drip infusions) to avoid possible loss of proteins.

The greatest effectiveness of detoxification is achieved with the combined use of several methods and the use of various biological media (blood, lymph) for cleansing.

Pathogenetic treatment of endotoxemia consists of the use of antiproteolytic drugs (contrical, trasylol or ingitril), antioxidants (tocopherol), immunostimulants (T-activin).

Ultraviolet irradiation of blood in a dose of up to 100-120 has the greatest effect in this regard. J, carried out daily in the amount of 5-6 procedures.

Detoxification and pathogenetic treatment should be carried out under the control of the dynamics of the concentration of SM and other laboratory indicators of endotoxemia until they are stable and normalized.

Forecast is largely related to the possibilities of using modern methods of artificial detoxification in the early stages of the development of endotoxemia.

While studying the topic, the student must have the following professional competencies:

Able and willing to identify critical disability in surgical patients

Able and willing to provide first aid for critical life events

I. Motivation for the purpose of the lesson

Knowledge of critical disabilities is necessary not only for the professional activities of a doctor of any specialty, but also in a person’s everyday life, because allows you to master methods of providing timely and targeted assistance in case of an accident in any conditions.

II. The purpose of self-training. To study the clinical signs and principles of medical care for conditions such as acute respiratory failure, acute cardiovascular failure, acute renal and liver failure, multiple organ failure syndrome.

III. Educational-target tasks

After independently studying the material on this topic, the student must

Know:

Ø clinical manifestations of acute respiratory failure;

Ø clinical manifestations of acute heart failure;

Ø clinical manifestations of acute renal failure;

Ø clinical manifestations of acute liver failure;

Ø clinical manifestations of multiple organ failure syndrome.

Be able to:

Ø diagnose acute respiratory failure, acute heart failure, acute renal and liver failure, multiple organ failure syndrome based on clinical symptoms;

Ø diagnose clinical death;

Ø provide first aid for respiratory failure;

Ø provide first aid for heart failure;

Ø provide first aid for renal failure;

Ø provide first aid for liver failure.

Own:

Ø an algorithm for determining the type of critical condition and skills in providing first aid to sick adults and surgical teenagers.

IV. Initial level of knowledge

The student must repeat the concept of first aid, indicators of the state of the functions of vital organs (blood pressure, pulse, frequency and amplitude of respiratory movements, etc.).

V. Topic study plan

1. Clinical assessment of general condition.

2. Types of dysfunction of the body in surgical patients.

3. Causes, development mechanisms, principles of diagnosis and treatment of acute respiratory failure.

4. Causes, development mechanisms, principles of diagnosis and treatment of acute heart failure.

5. Causes, development mechanisms, principles of diagnosis and treatment of acute renal failure.

6. Causes, development mechanisms, principles of diagnosis and treatment of acute liver failure.

7. Causes, development mechanisms, principles of diagnosis and treatment of multiple organ failure syndrome.

1. Sumin, S.A. Emergency conditions: textbook. manual for medical students. universities / S.A. Sumin. 6th ed., revised. and additional - M.: MIA, 2006. - 799 p.: ill. (Educational literature for students of medical universities and departments).

2. Practical skills and abilities in the course “General Surgery”: textbook. a manual for students of all faculties / ed. B.S. Sukovatykh; GOU VPO "Kursk State Medical University", department. general surgery.-Kursk: Publishing house of KSMU, 2009.-175 p.: ill.

3. Multimedia course of lectures on general surgery for self-training of 3rd year students of the Faculty of Medicine Kursk KSMU 2012.

Electronic library of a medical university “Student Consultant” www/studmedib.ru

4. General surgery: textbook / Petrov S.V. - 3rd ed., revised. and additional - M.: GEOTAR-Media, 2010. - 768 p. : ill.

5. General surgery: textbook / Gostishchev V.K. - 4th ed., revised. and additional - M.: GEOTAR-Media, 2010. - 848 p.

VII. Questions for self-control

6. By what criteria is the general condition of the patient assessed?